• anal sphincter
• neurological impairment

We read the case report of Malouf and Kamm (Gut 2001;48:728–9) with interest. However, we disagree with some of the science and suggest an alternative explanation for their findings.

Firstly, there is much data to suggest that sympathetic innervation of the internal anal sphincter is in fact excitatory. The paper that they cite¹ (from their own institution) showed that noradrenaline, the principal postganglionic neurotransmitter of the sympathetic nervous system, caused contraction of this tissue in vitro. Operative in vivo studies of presacral nerve stimulation have indeed been contradictory, showing both an increase² and decrease³ in internal anal sphincter tone; this probably reflects little more than differences in stimulation parameters. However, sympathetic blockade effected either by infusion of the α adrenoceptor antagonist phentolamine⁴ or by high spinal anaesthesia⁵ produces a significant fall in internal anal sphincter tone. This is evidence of tonic, excitatory, sympathetic innervation of the internal anal sphincter, not of “extrinsic sympathetic drive which relaxes the sphincter”, as described by Malouf and Kamm.

Secondly, acetylcholine relaxes internal anal sphincter in vitro,⁶ an action blocked both by atropine and nitric oxide synthase inhibitors. This implies that acetylcholine, the principal postganglionic neurotransmitter of the parasympathetic nervous system, is inhibitory and acts via muscarinic receptors and its effects are mediated by nitric oxide. Low spinal anaesthesia has little effect on anal canal resting pressure, suggesting that there is negligible tonic parasympathetic discharge to the internal anal sphincter.⁵ We are not aware of any convincing data that enable Malouf and Kamm to make the unreferenced statement that there is “normal extrinsic parasympathetic excitatory [sic] drive to the internal anal sphincter”.

Finally, the anal canal normally remains closed at rest because of the tone of the internal anal sphincter, which contributes around 80% of resting anal pressure.⁷ Most of this contraction is attributable to intrinsic myogenic tone although there is some tonic sympathetic discharge, as outlined above. Malouf and Kamm describe the anus of a spinal cord injured patient as having “gaped after digital examination for several minutes” and state that this might reflect loss of “normal extrinsic parasympathetic excitatory [sic] drive to the internal anal sphincter”. A much simpler, and pharmacologically correct, explanation would be that digital examination of this patient evoked the rectoanal inhibitory reflex and induced internal sphincter relaxation. Indeed, we would dispute that normally “the anal canal remains closed before, during, and after examination”. When the fingertip passes into the rectum of a non-spinal injury patient, a definite relaxation of the internal anal sphincter is often felt. This is not normally sustained for minutes, and it is this abnormality that is interesting in the case they report. High resting pressures are often seen in spinally injured patients and many of them use digital rectal stimulation to aid defecation.⁸